Dynamics of pathological changes in brain tissue following cardiac arrest induced ischemia were evaluated using double tracer autoradiography of regional in vivo 45Ca uptake as respective indicator of ischemic and 3H leucine protein synthesis as measure of metabolic cell integrity. Observations on abnormal calcium accumulation suggested that they were related to 45Ca uptake by either injured but still living neurons and/or by reactive glial elements. 45Ca autoradiography demonstrated a high sensitivity of the nucleus reticularis thalami, hippocampal CA1 pyramidal layer, inferior colliculus, ventral thalamic nucleus, caudate nucleus, and parietal cortex to ischemic neuron injury. Regional 3H leucine incorporation revealed that an initially widespread inhibition of protein synthesis was followed by its considerable recovery. Observations in the hippocampal CA1 sector and in the ventral thalamic nucleus (VTN) suggested that a significant degree of protein synthesis, maintained at the late stage after postischemic recovery, was related to survival and regeneration of neurons and not to the presence of glial elements.